a small overview of DKA and HHS

1. Diabetic ketoacidosis
and hyperosmolar
hyperglycemic state
Made by shubham bhardwaj to
Dr. Tamar zerekidze

2. Definition
Diabetic ketoacidosis (DKA) can happen in
people with diabetes if their body starts
run out of insulin. When this happens,
harmful substances called ketones build up
in the body.
Hyperosmolar hyperglycemic state is a
life-threatening emergency
by marked elevation of blood glucose
and hyperosmolarity with little or no
ketosis.

3. Diabetic
ketoacidosis
 DKA may be the initial symptom complex that leads to a
diagnosis of type 1 DM, but more frequently it occurs in
individuals with established diabetes.
 Cerebral edema, an extremely serious complication of
DKA, is seen most frequently in children. Signs of
infection, which may precipitate DKA, should be sought
on physical examination, even in the absence of fever.

4. pathophysiology
 DKA results from relative or absolute
insulin deficiency combined with
counterregulatory hormone excess
(glucagon, catecholamines, cortisol, and
growth hormone). The increased levels of
glucagon and catecholamines in the face of
low insulin levels promote glycogenolysis.
Insulin deficiency also reduces levels of the
GLUT4 glucose transporter.

5. Clinical features
 Symptoms
 Nausea/vomiting
 Thirst/polyuria
 Abdominal pain
 Chest pain
 Physical findings
 Tachycardia
 Dehydration/hypotension
 Tachypnea/Kussmaul
respirations
 respiratory distress
 Abdominal tenderness

6. HYPEROSMOLAR
HYPERGLYCEMIC
STATE
 The prototypical patient with HHS is an elderly individual
with type 2 DM, with a several-week history of polyuria,
weight loss, and diminished oral intake that culminates in
mental confusion, lethargy, or coma.
 Sepsis, pneumonia, and other serious infections are
frequent precipitants and should be sought. In addition, a
debilitating condition (prior stroke or dementia) or social
situation that compromises water intake usually
contributes to the development of the disorder.

7. Pathophysiology
 Relative insulin deficiency and inadequate fluid intake are the underlying
causes of HHS. Hyperglycemia induces an osmotic diuresis that leads to
intravascular volume depletion, which is exacerbated by inadequate fluid
replacement.
 insulin deficiency is only relative and less severe than in DKA. Lower levels of
counterregulatory hormones and free fatty acids have been found in HHS
than in DKA in some studies.
 The patient with HHS is usually older, more likely to have mental status
changes, and more likely to have a life-threatening precipitating event with
accompanying comorbidities. Even with proper treatment, HHS has a
substantially higher mortality than DKA (up to 15% in some clinical series).

9. Diagnosis
Normal values DKA HHS
PH 7.35 to 7.45 <7.3 >7.3
hco3 22 to 28 meq <18 >18
RBS 140 - 180 mg/dl >250 >600
ketones increased Less or absent

10. Treatment
 short-acting insulin: IV 0.1units/kg/h
 Replace fluids: 2–3 L of 0.9% saline
 Fluid replacement should initially stabilize
the hemodynamic status of the patient (1–3
L of 0.9% normal saline over the first 2–3 h)
 Potassium repletion is usually necessary
and should be dictated by repeated
measurements of the serum potassium.
 IV insulin bolus of 0.05 units/kg followed
by IV insulin at a constant infusion rate of
0.05 units/kg per h.
DKA HHS

11. Case
example
 An 8 –year- old child was admitted to the hospital after the
diagnosis of pneumonia. He was started with IV antibiotics.
After 48 hours of admission mother tells the doctor the child
was drowsy and had poor oral intake.
 Spo2 – 98% room air
 Venous Blood gas analysis – ph – 7.2 , pco2 – 40 mmhg, hco3 –
15 meq
 Urine analysis- ketones present
 RBS – 300mg
 Plasma β-hydroxybutyrate present
 Treatment- saline drip
 insulin drip